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Medicine and Science in Sports and... Sep 2022Skeletal muscle plays a critical role in physical function and metabolic health. Muscle is a highly adaptable tissue that responds to resistance exercise (RE; loading)... (Review)
Review
Skeletal muscle plays a critical role in physical function and metabolic health. Muscle is a highly adaptable tissue that responds to resistance exercise (RE; loading) by hypertrophying, or during muscle disuse, RE mitigates muscle loss. Resistance exercise training (RET)-induced skeletal muscle hypertrophy is a product of external (e.g., RE programming, diet, some supplements) and internal variables (e.g., mechanotransduction, ribosomes, gene expression, satellite cells activity). RE is undeniably the most potent nonpharmacological external variable to stimulate the activation/suppression of internal variables linked to muscular hypertrophy or countering disuse-induced muscle loss. Here, we posit that despite considerable research on the impact of external variables on RET and hypertrophy, internal variables (i.e., inherent skeletal muscle biology) are dominant in regulating the extent of hypertrophy in response to external stimuli. Thus, identifying the key internal skeletal muscle-derived variables that mediate the translation of external RE variables will be pivotal to determining the most effective strategies for skeletal muscle hypertrophy in healthy persons. Such work will aid in enhancing function in clinical populations, slowing functional decline, and promoting physical mobility. We provide up-to-date, evidence-based perspectives of the mechanisms regulating RET-induced skeletal muscle hypertrophy.
Topics: Exercise; Humans; Hypertrophy; Mechanotransduction, Cellular; Muscle, Skeletal; Resistance Training
PubMed: 35389932
DOI: 10.1249/MSS.0000000000002929 -
Journal of Strength and Conditioning... May 2012Exercise-induced muscle damage (EIMD) occurs primarily from the performance of unaccustomed exercise, and its severity is modulated by the type, intensity, and duration... (Review)
Review
Exercise-induced muscle damage (EIMD) occurs primarily from the performance of unaccustomed exercise, and its severity is modulated by the type, intensity, and duration of training. Although concentric and isometric actions contribute to EIMD, the greatest damage to muscle tissue is seen with eccentric exercise, where muscles are forcibly lengthened. Damage can be specific to just a few macromolecules of tissue or result in large tears in the sarcolemma, basal lamina, and supportive connective tissue, and inducing injury to contractile elements and the cytoskeleton. Although EIMD can have detrimental short-term effects on markers of performance and pain, it has been hypothesized that the associated skeletal muscle inflammation and increased protein turnover are necessary for long-term hypertrophic adaptations. A theoretical basis for this belief has been proposed, whereby the structural changes associated with EIMD influence gene expression, resulting in a strengthening of the tissue and thus protection of the muscle against further injury. Other researchers, however, have questioned this hypothesis, noting that hypertrophy can occur in the relative absence of muscle damage. Therefore, the purpose of this article will be twofold: (a) to extensively review the literature and attempt to determine what, if any, role EIMD plays in promoting skeletal muscle hypertrophy and (b) to make applicable recommendations for resistance training program design.
Topics: Exercise; Humans; Hypertrophy; Inflammation; Insulin-Like Growth Factor I; Muscle, Skeletal; Neutrophils; Satellite Cells, Skeletal Muscle; Signal Transduction
PubMed: 22344059
DOI: 10.1519/JSC.0b013e31824f207e -
Practical Neurology Oct 2017The physical examination always begins with a thorough inspection and patients with potential neuromuscular weakness are no exception. One question neurologists... (Review)
Review
The physical examination always begins with a thorough inspection and patients with potential neuromuscular weakness are no exception. One question neurologists routinely address during this early part of the assessment is whether or not there is muscle enlargement. This finding may reflect true muscle hypertrophy-myofibres enlarged from repetitive activity, for example, in myotonia congenita or neuromyotonia-or muscles enlarged by the infiltration of fat or other tissue termed pseudohypertrophy or false enlargement. Pseudohypertrophic muscles are frequently paradoxically weak. Recognising such a clinical clue at the bed side can facilitate a diagnosis or at least can narrow down the list of potential suspects. This paper outlines the conditions, both myopathic and neurogenic, that cause muscle enlargement.
Topics: Humans; Hypertrophy; Muscle, Skeletal; Muscular Diseases
PubMed: 28778933
DOI: 10.1136/practneurol-2017-001695 -
Medicine and Science in Sports and... Aug 1988It is widely believed that women experience less skeletal muscle hypertrophy consequent to heavy-resistance training than men. The purpose of this study was to test this...
It is widely believed that women experience less skeletal muscle hypertrophy consequent to heavy-resistance training than men. The purpose of this study was to test this hypothesis using both traditional indirect indicators as well as a direct measure of muscle size. Seven male experimental (ME), 8 female experimental (FE), and 7 control subjects were studied before and after a 16-wk weight training program, in which ME and FE trained 3 days.wk-1 at 70 to 90% of maximum voluntary contraction using exercise designed to produce hypertrophy of the upper arm and thigh. Strength increased significantly (P less than 0.05) in ME and FE, respectively, on elbow flexion (36.2 and 59.2%), elbow extension (32.6 and 41.7%), knee flexion (12.8 and 24.4%), and knee extension (28.8 and 33.9%) tests. Absolute changes were significantly greater in ME than FE in 2 of the 4 tests, whereas percentage changes were not significantly different. Substantial muscle hypertrophy occurred in the upper arms of both ME and FE as evidenced by significant increases in upper arm circumference (7.9 and 7.9%), bone-plus-muscle (B+M) cross-sectional area (CSA) estimated by anthropometry (17.5 and 20.4%), and muscle CSA determined from computed tomography scanning (15.9 and 22.8%). Changes by ME and FE were not significantly different, except for the absolute increase in estimated B+M CSA, which was significantly greater in ME (11.2 vs 7.4 cm2). No muscle hypertrophy occurred in the thigh of either ME and FE as evidenced by non-significant changes in thigh circumference (1.7 and 2.3%), B+M CSA (4.9 and 6.1%), and muscle CSA (2.9 and 2.9%). Changes by ME and FE in body weight, fat-free weight, and fat weight were not significant.(ABSTRACT TRUNCATED AT 250 WORDS)
Topics: Adipose Tissue; Adult; Anthropometry; Body Composition; Female; Humans; Hypertrophy; Male; Muscles; Sex Factors; Sports; Tomography, X-Ray Computed; Weight Lifting
PubMed: 3173042
DOI: 10.1249/00005768-198808000-00003 -
Biochimica Et Biophysica Acta.... Sep 2020Skeletal muscle is a dynamic tissue with two unique abilities; one is its excellent regenerative ability, due to the activity of skeletal muscle-resident stem cells... (Review)
Review
Skeletal muscle is a dynamic tissue with two unique abilities; one is its excellent regenerative ability, due to the activity of skeletal muscle-resident stem cells named muscle satellite cells (MuSCs); and the other is the adaptation of myofiber size in response to external stimulation, intrinsic factors, or physical activity, which is known as plasticity. Low physical activity and some disease conditions lead to the reduction of myofiber size, called atrophy, whereas hypertrophy refers to the increase in myofiber size induced by high physical activity or anabolic hormones/drugs. MuSCs are essential for generating new myofibers during regeneration and the increase in new myonuclei during hypertrophy; however, there has been little investigation of the molecular mechanisms underlying MuSC activation, proliferation, and differentiation during hypertrophy compared to those of regeneration. One reason is that 'degenerative damage' to myofibers during muscle injury or upon hypertrophy (especially overloaded muscle) is believed to trigger similar activation/proliferation of MuSCs. However, evidence suggests that degenerative damage of myofibers is not necessary for MuSC activation/proliferation during hypertrophy. When considering MuSC-based therapy for atrophy, including sarcopenia, it will be indispensable to elucidate MuSC behaviors in muscles that exhibit non-degenerative damage, because degenerated myofibers are not present in the atrophied muscles. In this review, we summarize recent findings concerning the relationship between MuSCs and hypertrophy, and discuss what remains to be discovered to inform the development and application of relevant treatments for muscle atrophy.
Topics: Animals; Biomarkers; Cell Proliferation; Humans; Hypertrophy; Muscle, Skeletal; Regeneration; Satellite Cells, Skeletal Muscle
PubMed: 32417255
DOI: 10.1016/j.bbamcr.2020.118742 -
Journal of Applied Physiology... Jan 2007The onset of whole muscle hypertrophy in response to overloading is poorly documented. The purpose of this study was to assess the early changes in muscle size and... (Clinical Trial)
Clinical Trial
The onset of whole muscle hypertrophy in response to overloading is poorly documented. The purpose of this study was to assess the early changes in muscle size and architecture during a 35-day high-intensity resistance training (RT) program. Seven young healthy volunteers performed bilateral leg extension three times per week on a gravity-independent flywheel ergometer. Cross-sectional area (CSA) in the central (C) and distal (D) regions of the quadriceps femoris (QF), muscle architecture, maximal voluntary contraction (MVC), and electromyographic (EMG) activity were measured before and after 10, 20, and 35 days of RT. By the end of the training period, MVC and EMG activity increased by 38.9 +/- 5.7 and 34.8% +/- 4.7%, respectively. Significant increase in QF CSA (3.5 and 5.2% in the C and D regions, respectively) was observed after 20 days of training, along with a 2.4 +/- 0.7% increase in fascicle length from the 10th day of training. By the end of the 35-day training period, the total increase in QF CSA for regions C and D was 6.5 +/- 1.1 and 7.4 +/- 0.8%, respectively, and fascicle length and pennation angle increased by 9.9 +/- 1.2 and 7.7 +/- 1.3%, respectively. The results show for the first time that changes in muscle size are detectable after only 3 wk of RT and that remodeling of muscle architecture precedes gains in muscle CSA. Muscle hypertrophy seems to contribute to strength gains earlier than previously reported; flywheel training seems particularly effective for inducing these early structural adaptations.
Topics: Adolescent; Adult; Electromyography; Ergometry; Exercise; Female; Humans; Hypertrophy; Magnetic Resonance Imaging; Male; Muscle Contraction; Muscle, Skeletal; Time Factors; Weight Lifting
PubMed: 17053104
DOI: 10.1152/japplphysiol.00789.2006 -
American Journal of Physiology.... Jan 2022Macrophages are one of the top players when considering immune cells involved with tissue homeostasis. Recently, increasing evidence has demonstrated that macrophages... (Review)
Review
Macrophages are one of the top players when considering immune cells involved with tissue homeostasis. Recently, increasing evidence has demonstrated that macrophages could also present two major subsets during tissue healing: proliferative macrophages (M1-like), which are responsible for increasing myogenic cell proliferation, and restorative macrophages (M2-like), which are involved in the end of the mature muscle myogenesis. The participation and characterization of these macrophage subsets are critical during myogenesis to understand the inflammatory role of macrophages during muscle recovery and to create supportive strategies that can improve mass muscle maintenance. Indeed, most of our knowledge about macrophage subsets comes from skeletal muscle damage protocols, and we still do not know how these subsets can contribute to skeletal muscle adaptation. Thus, this narrative review aims to collect and discuss studies demonstrating the involvement of different macrophage subsets during the skeletal muscle damage/regeneration process, showcasing an essential role of these macrophage subsets during muscle adaptation induced by acute and chronic exercise programs.
Topics: Animals; Cell Proliferation; Exercise; Humans; Hypertrophy; Inflammation; Inflammation Mediators; Macrophages; Muscle, Skeletal; Phenotype; Regeneration; Signal Transduction; Skeletal Muscle Enlargement
PubMed: 34786967
DOI: 10.1152/ajpregu.00038.2021 -
Anatomy and Embryology 1990Smooth muscles of viscera undergo a large increase in volume when there is a chronic, partial obstruction impairing the flow of lumenal contents. Hypertrophy of smooth... (Review)
Review
Smooth muscles of viscera undergo a large increase in volume when there is a chronic, partial obstruction impairing the flow of lumenal contents. Hypertrophy of smooth muscle occurs in various medical conditions and several methods are available for inducing it experimentally in laboratory animals, especially in urinary bladder, small intestine and ureter. The hypertrophic response differs somewhat with the type of organ, the animal species, the age of the subject, and the experimental procedure. Ten- to fifteen-fold increases in muscle volume develop within a few weeks in the urinary bladder or the ileum of adult animals, a growth that would not have occurred in the lifespan of the animal without the experimental intervention. The general architecture of the muscle and the boundaries with adjacent tissues are well preserved. In intestinal hypertrophy, muscle cells increase in number: mitoses are found in mature, fully differentiated muscle cells. Cell division by full longitudinal splitting of muscle cells may also occur. Enlargement of muscle cells accounts for most of the muscle hypertrophy. The hypertrophic muscle cell has an irregular profile with deep indentations of the cell membrane, bearing caveolae and dense bands; however, the cell surface grows less than the cell volume (reduction of surface-to-volume ratio). The nucleus is crenated and is much less enlarged than the cell (reduction of the nucleo-plasmatic ratio). Mitochondria grow in number but in some muscles their spatial density decreases; intermediate filaments increase more than myofilaments. The spatial density of sarcoplasmic reticulum is generally increased. In the hypertrophic intestine, gap junctions increase in number and size; in the bladder, gap junctions are absent both in control and in hypertrophy. Thus the hypertrophic muscle cell is not only larger than a control cell, but has a different pattern of its structural components. Extensive neo-angiogenesis maintains a good blood supply to the hypertrophic muscle. The density of innervation is much decreased in the hypertrophic intestine, whereas it appears well maintained in the bladder. Neuronal enlargement is found in the intramural ganglia of the intestine and in the pelvic ganglion. The mechanisms involved in hypertrophic growth are unknown. Three possible factors, mechanical factors, especially stretch, altered nerve discharge, and trophic factors are discussed.
Topics: Animals; Humans; Hypertrophy; Muscle, Smooth; Viscera
PubMed: 2291488
DOI: 10.1007/BF00178906 -
European Journal of Applied Physiology May 2020Resistance exercise induces muscle growth and is an important treatment for age-related losses in muscle mass and strength. Myokines are hypothesized as a signal... (Review)
Review
PURPOSE
Resistance exercise induces muscle growth and is an important treatment for age-related losses in muscle mass and strength. Myokines are hypothesized as a signal conveying physiological information to skeletal muscle, possibly to "fine-tune" other regulatory pathways. While myokines are released from skeletal muscle following contraction, their role in increasing muscle mass and strength in response to resistance exercise or training is not established. Recent research identified both local and systemic release of myokines after an acute bout of resistance exercise. However, it is not known whether myokines with putative anabolic function are mechanistically involved in producing muscle hypertrophy after resistance exercise. Further, nitric oxide (NO), an important mediator of muscle stem cell activation, upregulates the expression of certain myokine genes in skeletal muscle.
METHOD
In the systemic context of complex hypertrophic signaling, this review: (1) summarizes literature on several well-recognized, representative myokines with anabolic potential; (2) explores the potential mechanistic role of myokines in skeletal muscle hypertrophy; and (3) identifies future research required to advance our understanding of myokine anabolism specifically in skeletal muscle.
RESULT
This review establishes a link between myokines and NO production, and emphasizes the importance of considering systemic release of potential anabolic myokines during resistance exercise as complementary to other signals that promote hypertrophy.
CONCLUSION
Investigating adaptations to resistance exercise in aging opens a novel avenue of interdisciplinary research into myokines and NO metabolites during resistance exercise, with the longer-term goal to improve muscle health in daily living, aging, and rehabilitation.
Topics: Cytokines; Exercise; Humans; Hypertrophy; Muscle, Skeletal; Resistance Training
PubMed: 32144492
DOI: 10.1007/s00421-020-04337-1 -
JCI Insight Aug 2023The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic...
The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic reticulum (ER) is largely unknown. Here, we report that the SEL1L-HRD1 ER-associated degradation (ERAD) complex, the primary molecular machinery that degrades misfolded proteins in the ER, is vital to maintain postnatal muscle growth and systemic energy balance. Myocyte-specific SEL1L deletion blunts the hypertrophic phase of muscle growth, resulting in a net zero gain of muscle mass during this developmental period and a 30% reduction in overall body growth. In addition, myocyte-specific SEL1L deletion triggered a systemic reprogramming of metabolism characterized by improved glucose sensitivity, enhanced beigeing of adipocytes, and resistance to diet-induced obesity. These effects were partially mediated by the upregulation of the myokine FGF21. These findings highlight the pivotal role of SEL1L-HRD1 ERAD activity in skeletal myocytes for postnatal muscle growth, and its physiological integration in maintaining whole-body energy balance.
Topics: Humans; Endoplasmic Reticulum-Associated Degradation; Ubiquitin-Protein Ligases; Proteins; Muscles; Energy Metabolism; Hypertrophy
PubMed: 37535424
DOI: 10.1172/jci.insight.170387